Percorrer por autor "Abrantes, Leonor"
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- Activation of RAC1/PAK1 axis potentiates transcriptional upregulation of DNA damage response genes via the BCL6/STAT5 switchPublication . Barros, Patrícia; Amaral, Andreia; Abrantes, Leonor; Oliveira, Tiago; Lourio, Henriqueta; Silva, Maria João; Jordan, Peter; Gama-Carvalho, Margarida; Matos, PauloColorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in colorectal cancers, particularly those with more aggressive and invasive features, leading to unfavourable clinical prognosis, often resulting from chemoresistance.
- Familial Chylomicronemia Syndrome: clinical and molecular characterization of individuals WITH clinical diagnosis in PortugalPublication . Alves, Ana Catarina; Abrantes, Leonor; Sequeira, Sílvia; Moldovan, Oana; Nunes, Catarina; Antunes, Henedina; Martins, Esmeralda; Gonçalves, Rute; Duarte, Sequeira; Guerra, António; Gaspar, Ana; Salgado, Miguel; Azevedo, Aida; Rato, Quitéria; Palma, Isabel; Bourbon, MafaldaAim: Familial chylomicronemia syndrome (FCS) is a rare autosomal recessive disorder of lipoprotein metabolism. It is characterized by marked elevation of triglyceride and chylomicron levels, lipaemic plasma, recurrent pancreatitis, eruptive xanthoma, hepatosplenomegaly, and liapemia retinalis. All genes associated with FCS (LPL, APOC2, APOA5, LMF1 and GPHBP1) have an effect on the activity of lipoprotein lipase (LPL). The aim of this study is to present all cases with FCS clinical diagnosis, studied in our laboratory.
- Stimulation of RAC1/PAK1 signalling upregulates DNA damage repair genes via STAT5 stimulation of BCL6 repressed lociPublication . Barros, Patrícia; Amaral, Andreia; Abrantes, Leonor; Oliveira, Tiago; Louro, Henriqueta; Silva, Maria João; Jordan, Peter; Gama-Carvalho, Margarida; Matos, PauloColorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in colorectal cancers, particularly those with more aggressive and invasive features, leading to unfavourable clinical prognosis, often resulting from chemoresistance.
- Stimulation of RAC1/PAK1 signalling upregulates DNA damage repair genes via STAT5 stimulation of BCL6 repressed lociPublication . Barros, Patricia; Amaral, Andreia; Abrantes, Leonor; Oliveira, Tiago; Louro, Henriqueta; Silva, Maria joão; Jordan, Peter; Gama-Carvalho, Margarida; Matos, PauloColorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in colorectal cancers, particularly those with more aggressive and invasive features, leading to unfavourable clinical prognosis, often resulting from chemoresistance.
- Stimulation of RAC1/PAK1 signalling upregulates DNA damage repair genes via the BCL6/STAT5-switchPublication . Barros, Patrícia; Amaral, Andreia; Abrantes, Leonor; Oliveira, Tiago; Louro, Henriqueta; Silva, Maria João; Jordan, Peter; Gama-Carvalho, Margarida; Matos, PauloColorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in colorectal cancers, particularly those with more aggressive and invasive features, leading to unfavourable clinical prognosis, often resulting from chemoresistance.
- Upregulation of RAC1/PAK1 signalling promotes DNA damage repair in colorectal cancer cellsPublication . Barros, Patricia; Amaral, Andreia; Abrantes, Leonor; Oliveira, Tiago; Louro, Henriqueta; Silva, Maria Joâo; Jordan, Peter; Gama Carvalho, Margarida; Matos, PauloIntroduction: Colorectal cancer is one of the most prevalent types of cancer worldwide. The GTPase RAC1 and its effector PAK1 have been found overexpressed or hyperactivated in this type of cancers, particularly those with more aggressive and invasive features, which is frequently correlated with resistance to chemotherapeutics and unfavourable clinical prognosis. Previously, we described a new signalling pathway in which activation of RAC1/PAK1 signalling promotes a transcriptional switch between the BCL6 repressor and the STAT5 transcriptional activator at a restricted subset of gene promoters.